1. Field of the Invention:
This invention relates to drugs and foods useful in the therapy of patients suffering from alcoholic hepatic disorders as well as its prevention.
2. Discussion of the Background:
The excessive ingestion of alcoholic (ethanolic) beverages chronically elicits various diseases, especially hepatic disorders and dysfunctions, such as fatty liver, alcoholic hepatitis, cirrhosis and so on. The liver is attacked because ethanol is catabolized specifically in this organ.
Total abstinence from alcoholic beverages is strongly recommended to patients with alcoholic hepatic disorders. These patients also receive therapy with drugs containing vitamins, phospholipids, glucocorticoids or insulin. In addition, drugs containing glucuronate or an amino acid, for example, L-arginine hydrochloride, are available to treat these patients.
Nonetheless, these treatments and prescriptions often fail to provide a complete regression of the disease. This is at least in part due to the fact that the patients still indulge in an occasional drink despite strongly recommended total abstinence.
Recently, it has become clear that some amino acids, for example, Ala etc., are quite potent at enhancing the survival rate of mice who have received a lethal dose of ethanol. In particular, concurrent treatment with Ala and L-ornithine has been reported to be synergistically effective (Petition for Japanese patent, Showa No. 61-50917).
It can also be recognized that rats display a preference for Ala as well as for Gln under dietary ethanol loading for periods of time (6 months or more), and that pretreatment of rats with both compounds ameliorated either ethanol clearance from the blood or recovery from a comatose state and the subsequent depression behavior which follows the ethanol loading. But these facts cannot be extrapolated to determine if a therapy of Ala and Gln for a progressed state of alcoholic hepatic disorders is effective or not.
It is known that the dizziness experienced after drinking is closely related to the concentration of acetoaldehyde in the drinker's blood. The concentration of this metabolite of ethanol in the blood is substantially elevated after drinking. Pretreatment with Ala, L-glutamate or aspartate decreases the toxicity of acetoaldehyde as a catabolite of ethanol, but does not suppress serum enzymatic activities, which are released from a damaged liver by ethanol loading, has ever occurred (Petition of Japanese patent, Showa No. 61-134313).
Therapy for patients suffering from alcoholic hepatic disorders induced by the excessive ingestion of ethanolic beverages has usually focused on attempts to ameliorate the degree of hepatic damage, mainly the parenchymal cell. However a complete regression is difficult for patients when the condition of the liver becomes worse and chronic. In addition, it is very hard to normalize serum enzymatic activity which is elevated by alcoholic hepatic damage because patients still indulge in drinking. Drugs for the hepatic damage and its prevention have been sought.
In view of the fact that the excessive consumption of alcoholic beverages is a widespread international phenomenon, there is a strongly felt need for a composition useful for therapy in the treatment of hepatic disorders and/or its prevention.